Hypoesthesia or absence

Introduction Diabetic peripheral neuritis (polyneuritis in diabetes) sensory disorder with shallow sensation diminished or disappeared, can also be expressed as hyperesthesia, often accompanied by a variety of paresthesia such as acupuncture pain, burning pain or cold pain, ants walking and Numbness.

Cause

(1) Causes of the disease

The underlying cause of diabetic peripheral neuropathy is that diabetes is not effectively controlled, leading to peripheral neuropathy. This is one of the most common chronic complications of diabetes, its clinical manifestations are diverse, and its mechanisms of action are diverse. It is currently difficult to explain such diverse neuropathy with a single mechanism. The combined effects of multiple pathological mechanisms may ultimately lead to complex and variable clinical manifestations.

(two) pathogenesis

Metabolic disorder theory

(1) Tissue glycosylation: elevated blood glucose can cause glycosylation of tissue proteins, and glycosylation protein end products are not only an important factor causing systemic complications of diabetes, but also destroy the myelin structure of peripheral nerves. Causes the loss of myelin. Glycosylation of microfilaments and tubulin can result in axonal degeneration. The glycosylation process of this tissue protein in diabetic patients can continue after the blood glucose level returns to normal, resulting in persistent peripheral nerve damage.

(2) Inositol metabolism abnormality: Inositol is a substrate for the synthesis of phosphatidylinositol, and phosphatidylinositol can not only affect the activity of cell membrane Na-K-ATPase, but also an important substance for cell transmembrane information transmission. Cellular intake of inositol requires a Na-dependent carrier. Inositol is similar in structure to glucose. Hyperglycemia competitively inhibits Na-dependent carriers, reduces inositol uptake by cells, and reduces intracellular inositol levels. Affects nerve structure and function.

(3) sorbitol fructose metabolism disorder: hyperglycemia can increase the activity of aldose reductase in peripheral nerve Schwann (Swanwang) cells, accelerate the process of glucose conversion to sorbitol, and sorbitol in sorbitol dehydrogenase Oxidation to produce fructose, which causes excessive accumulation of sorbitol and fructose in the cells, causing an increase in intracellular osmotic pressure and retention of sodium and water, resulting in deterioration of peripheral nerve neuronal cells (Schwann cells), loss of myelin and axonal mutation. Sex.

2. Microcirculatory disorders theory

(1) Microvascular disease and ischemia and hypoxia: Hyperglycemia can cause glycosylation of microvascular structural proteins, resulting in vascular endothelial proliferation, thickening of the intima, hyaline degeneration and thickening of the basement membrane, and increased capillary permeability. Severe cases can cause vascular stenosis, and even thrombosis, causing ischemia and hypoxia damage to peripheral nerve tissue. A comparative study of wrinkle circulation in patients with diabetes mellitus and diabetes mellitus complicated with peripheral neuropathy showed that the visibility of microcirculation in diabetic patients with peripheral neuropathy was significantly reduced, the visual field was dark red, most of the tube sputum was blurred, and the number was reduced. The sputum becomes thin and short and the visible input sputum and microangioma exist, and it permeates around the periorbital. The blood flow velocity is obviously slowed down, and it is in a sediment-like agglomeration flow state.

(2) Reduction of vasoactive factors: vascular vasoactive factors (NO) in diabetic peripheral neuropathy are reduced, endothelium nourishment vessels are less sensitive to vasodilation factors, and smooth muscle diastolic function is abnormal, resulting in microcirculatory disorders. In addition, the abnormal metabolism of arachidonic acid causes a decrease in the ratio of prostacyclin (PGl2) and thromboxane (TXA2), vasoconstriction, and hypercoagulability of the blood, resulting in ischemia and hypoxia of the nerve tissue.

3. Immunological mechanism studies have shown that 12% of patients with diabetic peripheral neuropathy are positive for serum anti-GM1 antibodies and are associated with distal symmetric polyneuropathy. 88% of patients were positive for antiphospholipid antibodies, while only 32% of diabetic patients without neurological complications were positive for this antibody. It indicates that the pathogenesis of diabetic peripheral neuropathy is related to autoimmunity.

The main pathological features of diabetic peripheral neuropathy are axonal degeneration and segmental demyelination, accompanied by significant remyelination and unmyelinated fibroplasia. Studies on the spatial distribution of sciatic nerve, sural nerve and vagus neuropathy showed that both axonal degeneration and demyelination were reverse dying, that is, the distal axonal degeneration was heavier and the proximal end was relatively light. Multiple segmental myelination can be either primary or secondary. Some patients have pathological features of hypertrophic neuropathy, which is characterized by Schwann cell proliferation forming an onion-like structure, and collagen fibrosis is observed with collagen sac formation. Cochlear nerve biopsy in patients with clinical manifestations of painful neuropathy showed selective fine myelinated fiber loss with unintentional fiber axis sprouting. Autopsy pathological observations of diabetic peripheral neuropathy can sometimes reveal the loss of posterior root ganglion cells and anterior horn cells and the axonal degeneration of nerve roots and posterior cords.

Vascular lesions are one of the pathological features of diabetic peripheral neuropathy. The outer membrane of the outer membrane and the small intima of the intima were swollen, the lumen was narrowed or even occluded, and the adventitia was thickened with mononuclear cell infiltration. Basal membrane thickening is another pathological feature of diabetic peripheral neuropathy. The basement membrane at the nerve bundle membrane, Schwann cells and vascular endothelial cells can be significantly thickened, with the most prominent of the nerve bundle membrane. The longer the long-term sympathetic neuropathy, the more obvious the basement membrane thickening, and the milder single neuropathy is less severe.

an examination

Related inspection

Positional blood routine

1. Determination of blood sugar and glucose tolerance.

2. Other blood tests include routine examination of liver function, renal function, and erythrocyte sedimentation rate; rheumatoid series, immunoglobulin electrophoresis, and other serological tests related to autoimmunity.

3. Detection of serum heavy metals (lead, mercury, arsenic, antimony, etc.).

4. Urine examination includes urine sugar, urine routine, local-peripheral protein, urinary porphyrin and heavy metal excretion in urine.

5. Cerebrospinal fluid examination.

6. Electromyography and neurophysiological examination.

7. Organize biopsies (including skin, sural nerves, muscles, and kidneys) as necessary to identify other sensory peripheral neuropathies.

Differential diagnosis

The first is the diagnosis and identification of diabetes. Secondly, the disease should be differentiated from other sensory peripheral neuropathy and painful peripheral neuropathy. Diabetic muscular atrophy should be caused by quadriceps muscle myopathy, progressive spinal muscular atrophy, and lumbosacral radiculopathy. Identification of muscle atrophy.

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